This specification relates generally to acoustic therapies for the treatment of various conditions, such as sound sensitivities, behavioral and autonomic state regulation difficulties, atypical social engagement behaviors and/or auditory processing deficits.
Sound sensitivities, difficulties in behavioral and autonomic state regulation, atypical social engagement behaviors and auditory processing deficits are prevalent symptoms in autism spectrum disorders (“ASD”) and other psychiatric diagnoses, such as Post-traumatic stress disorder (“PTSD”). These symptoms may also be present in individuals with developmental disabilities (e.g., Fragile X Syndrome, Prader Willi Syndrome), as well as in aging individuals and those who have been subjected to abuse or neglect.
Sound sensitivities may be experienced as a discomfort with background ambient sounds or a sensitivity to specific sounds. Such symptoms may be dependent or independent of sound source or the specific frequencies and/or loudness of sound. Problems in state regulation may be expressed as atypical autonomic regulation, atypical social and emotional behaviors, low reactivity thresholds, chronic pain, tantrums, difficulties in sustaining attention and/or sleep disorders. And auditory processing deficits may be experienced as language and speech delays, difficulties in extracting human voice from background sounds and/or as a general compromise in social communication skills.
The mechanisms mediating sound sensitivities, autonomic and behavioral state regulation, social engagement and auditory processing are generally assumed to represent disparate response systems. From an empirical perspective, behavioral state regulation and social engagement are manifested in observable behaviors; autonomic regulation is observed in peripheral physiological reactions and medical systems; sound sensitivities are manifested through subjective experiences; and auditory processing is manifested in expressive and/or receptive language skills. Because sound sensitivities and deficits in state regulation, social engagement, and auditory processing lack diagnostic specificity, researchers who study the neurobiological and biobehavioral features of a specific psychiatric diagnosis (e.g., ASD, PTSD, etc.) or a genetic-based neurodevelopment disorder (e.g., Fragile X Syndrome, Prader Willi Syndrome, etc.) have not focused on these domains.
Moreover, sound sensitivities, behavioral and autonomic state regulation, social engagement and auditory processing are dependent on response systems that are studied by different scientific disciplines, which have little interaction and virtually no common language. For example, the study of psychiatric disorders (i.e., diagnoses), autonomic state regulation problems (e.g., symptoms manifested in visceral organs such as cardiovascular or digestive disorders), behavioral problems (e.g., state regulation and tantrums), psychological difficulties (e.g., emotional instability), sound sensitivities (e.g., a general or selective hypersensitivity to sounds), auditory processing disorders (e.g., difficulties understanding verbal instructions), and cognitive deficits (e.g., language delays) represent research domains investigated by separate disciplines. These distinctions contribute to conventional models of inquiry applied in clinical neuroscience, which rely on separate disciplines to categorize, investigate, treat, and explain the neurobiological mechanisms of clinical disorders.
One particular theory, the Polyvagal Theory, proposes a strategy that applies evolution as an organizing principle to understand a link between sound sensitivities, behavioral and autonomic state regulation, social engagement and auditory processing. According to the Polyvagal Theory, the well-documented phylogenetic shift in neural regulation of the autonomic nervous system provided mammals with a neural circuit that promotes social interactions in safe contexts by supporting calm physiological states and an ability to process relatively soft vocalizations in a frequency band distinct from the lower frequencies associated with reptilian predators. This “mammalian” circuit functions as the neural substrate for an integrated, social engagement system that dampens the functional impact of sounds outside the frequency band of vocalizations employed for social communication and regulates the neural circuits that optimize behavioral state, social engagement, and auditory processing.
An exemplary social engagement system according to the Polyvagal Theory is illustrated in FIG. 1. As shown, the social engagement system 100 includes a somatomotor component 140 with special visceral efferent pathways traveling through five cranial nerves 130 (i.e., the trigeminal nerve (V), facial nerve (VII), glossopharyngeal nerve (IX), vagus nerve (X) and accessory nerve (XI)) that regulate the striated muscles of the face and head (e.g., middle-ear muscles 141, laryngeal muscles 142, muscles of mastication 143, facial muscles 144, pharyngeal muscles 145 and head-turning muscles 146). The somatomotor component 140 regulates the pitch of vocalizations, the tension on the middle-ear muscles to enhance detection and processing of vocalizations, and facial expressions that supplement communicated messages and allow a listener to provide feedback to a vocalizer.
The social engagement system 100 also includes a visceromotor component 150 with the myelinated vagus that regulates the heart 151 and bronchi 152 to adjust an individual's physiological state to be complement their facial and vocal signals of social communication. Thus, the visceromotor component 150 allows for an individual to project a physiological state of calmness or defense through voice and face. Coincident with this projection of physiological state, the middle-ear muscles change muscle tone to either facilitate the processing of vocalizations (e.g., by dampening the transfer of acoustic energy representing low frequencies in the background) or enhance the processing of low frequency acoustic energy at the expense of dampening the ability to extract the acoustic information of vocalizations. Because, via evolution, low-frequency acoustic information signaled predator or environmental danger, this system requires cues of “safety.”
Based on the Polyvagal Theory, sound sensitivities and deficits in state regulation, social engagement and auditory processing may be paralleled by reduced vagal influences to the heart and bronchi via myelinated vagal pathways. Such a reduction is an adaptive response strategy to support mobilization (i.e., so-called “fight-flight” behaviors) in dangerous environments. Since the Polyvagal Theory articulates a hierarchy of neural circuits, the metabolic resources necessary for fight-flight behaviors are not efficiently available unless there is a retraction of the vagal brake—a calming mechanism that functions via the myelinated vagus to slow heart rate, optimize oxygenation of the blood, and to downregulate the sympathetic nervous system. This neurophysiological calming mechanism downregulates defensive states and enables social engagement behaviors to spontaneously occur. Thus, the neural mechanisms defining the social engagement system provide a plausible model to explain why sound sensitivities and both auditory processing and state regulation difficulties are prevalent in individuals with ASD and other clinical disorders. Consistent with this model, features of the social engagement system become windows of assessment and, due to the integrated nature of the system, these features may also be portals for possible intervention.
One particular portal of interest lies in the neural regulation of the middle-ear muscles. These muscles facilitate the extraction of human speech by dampening the transmission of low-frequency noise from the external environment to the inner ear. Sound enters the outer ear and travels, through the external auditory canal, to the eardrum where it is transduced by the structures of the middle ear (i.e., small bones comprising the ossicular chain) that connect the eardrum with the cochlea.
The rigidity of the ossicular chain determines the stiffness of the eardrum, which, in part, determines the acoustic properties of sounds transmitted to the inner ear. The middle-ear muscles, via cranial nerves, regulate the position of the ossicles and stiffen or loosen the eardrum. When the eardrum is “tightened,” higher frequencies are absorbed and transmitted to the inner ear and the energy of lower frequencies is attenuated (i.e., reflected) before being encoded by the inner ear (i.e., the cochlea) and transmitted via the auditory nerve (i.e., cranial nerve VIII) to the cortex. Complementing the ascending pathways are descending pathways that regulate the middle-ear muscles, which functionally determine the energy (i.e., attenuate, pass, or amplify) of specific frequencies that reach the inner ear.
The features describing the transformation of sound intensity from the outer ear to the inner ear defines the middle-ear transfer function. If the acoustic information in the frequency band associated with speech is distorted by an atypical middle-ear transfer function, the information coded by the inner ear (and subsequently transmitted to the cortex) may not contain sufficient information to enable accurate detection of speech sounds. In addition, there are descending pathways that regulate the hair cells in the cochlea to fine tune auditory perception, which is especially important in the development of language skills. If the acoustic information related to human speech that reaches the cortex via ascending pathways is distorted, then the descending pathways to the cochlea may also be atypical and will further distort the individual's ability to process speech and to produce language.
Atypical central regulation of peripheral middle-ear structures may pass low-frequency sounds that dominate the acoustic spectrum in our mechanized society (e.g., ventilation systems, traffic, airplanes, vacuum cleaners, and other appliances). This may result in both a hypersensitivity to sounds and a distortion or “masking” of the frequency components associated with human speech reaching the brain. Thus, an atypical middle-ear transfer function may be a potentially parsimonious explanation of both the auditory hypersensitivities and the difficulties in auditory processing frequently associated with autism.
There is a need in the art for systems and methods that can rehabilitate the integrated social engagement system via exercise of a specific portal, such as the middle-ear muscles.